Government-Owned Inventions; Availability for Licensing, 46309-46311 [2015-19082]
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tkelley on DSK3SPTVN1PROD with NOTICES
Federal Register / Vol. 80, No. 149 / Tuesday, August 4, 2015 / Notices
Place: National Institutes of Health,
Building 31, 31 Center Drive, Conference
Room 10, Bethesda, MD 20892.
Contact Person: Brent B. Stanfield, Ph.D.,
Director, Division of Extramural Activities,
National Institutes of Diabetes And Digestive
and Kidney Diseases, 6707 Democracy Blvd.
Room 715, MSC 5452, Bethesda, MD 20892,
(301) 594–8843, stanfibr@niddk.nih.gov.
Name of Committee: National Diabetes and
Digestive and Kidney Diseases Advisory
Council; Kidney, Urologic and Hematologic
Diseases Subcommittee.
Date: September 9, 2015.
Open: 1:00 p.m. to 3:00 p.m.
Agenda: To review the Division’s scientific
and planning activities.
Place: National Institutes of Health,
Building 31, 31 Center Drive, Conference
Room 7, Bethesda, MD 20892.
Closed: 3:00 p.m. to 3:30 p.m.
Agenda: To review and evaluate grant
applications.
Place: National Institutes of Health,
Building 31, 31 Center Drive, Conference
Room 7, Bethesda, MD 20892.
Contact Person: Brent B. Stanfield, Ph.D.,
Director, Division of Extramural Activities,
National Institutes of Diabetes And Digestive
and Kidney Diseases, 6707 Democracy Blvd.
Room 715, MSC 5452, Bethesda, MD 20892,
(301) 594–8843, stanfibr@niddk.nih.gov.
Name of Committee: National Diabetes and
Digestive and Kidney Diseases Advisory
Council; Digestive Diseases and Nutrition
Subcommittee.
Date: September 9, 2015.
Open: 1:00 p.m. to 3:00 p.m.
Agenda: To review the Division’s scientific
and planning activities.
Place: National Institutes of Health,
Building 31, 31 Center Drive, Conference
Room 6, Bethesda, MD 20892.
Closed: 3:00 p.m. to 3:30 p.m.
Agenda: To review and evaluate grant
applications.
Place: National Institutes of Health,
Building 31, 31 Center Drive, Conference
Room 6, Bethesda, MD 20892.
Contact Person: Brent B. Stanfield, Ph.D.,
Director, Division Of Extramural Activities,
National Institutes of Diabetes And Digestive
and Kidney Diseases, 6707 Democracy Blvd.
Room 715, MSC 5452, Bethesda, MD 20892
(301) 594–8843, stanfibr@niddk.nih.gov.
Any interested person may file written
comments with the committee by forwarding
the statement to the Contact Person listed on
this notice. The statement should include the
name, address, telephone number and when
applicable, the business or professional
affiliation of the interested person.
In the interest of security, NIH has
instituted stringent procedures for entrance
onto the NIH campus. All visitor vehicles,
including taxicabs, hotel, and airport shuttles
will be inspected before being allowed on
campus. Visitors will be asked to show one
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visit.
Information is also available on the
Institute’s/Center’s home page:
www.niddk.nih.gov/fund/divisions/DEA/
Council/coundesc.htm., where an agenda and
VerDate Sep<11>2014
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any additional information for the meeting
will be posted when available.
(Catalogue of Federal Domestic Assistance
Program Nos. 93.847, Diabetes,
Endocrinology and Metabolic Research;
93.848, Digestive Diseases and Nutrition
Research; 93.849, Kidney Diseases, Urology
and Hematology Research, National Institutes
of Health, HHS)
Dated: July 29, 2015.
David Clary,
Program Analyst, Office of Federal Advisory
Committee Policy.
[FR Doc. 2015–19024 Filed 8–3–15; 8:45 am]
BILLING CODE 4140–01–P
DEPARTMENT OF HEALTH AND
HUMAN SERVICES
National Institutes of Health
Government-Owned Inventions;
Availability for Licensing
AGENCY:
National Institutes of Health,
HHS.
ACTION:
The inventions listed below
are owned by an agency of the U.S.
Government and are available for
licensing in the U.S. in accordance with
35 U.S.C. 209 and 37 CFR part 404 to
achieve expeditious commercialization
of results of federally-funded research
and development. Foreign patent
applications are filed on selected
inventions to extend market coverage
for companies and may also be available
for licensing.
FOR FURTHER INFORMATION CONTACT:
Licensing information and copies of the
U.S. patent applications listed below
may be obtained by writing to the
indicated licensing contact at the Office
of Technology Transfer, National
Institutes of Health, 6011 Executive
Boulevard, Suite 325, Rockville,
Maryland 20852–3804; telephone: 301–
496–7057; fax: 301–402–0220. A signed
Confidential Disclosure Agreement will
be required to receive copies of the
patent applications.
SUPPLEMENTARY INFORMATION:
Technology descriptions follow.
Interferon Alpha Hybrids
Description of Technology: Available
for licensing are hybrid interferon alpha
(INF-alpha) polypeptides constructed by
combinations of INFalpha21b and
INFalpha2c, and mutants of these
hybrids. These hybrid constructs have
resulted in novel IFNs that either
combine different biological properties
from the parent proteins or have
significantly different biological activity
from both the parents in antiproliferative, anti-viral, or competitive
Frm 00076
Fmt 4703
binding properties. For instance, the
hybrid designated HY–3 has higher antiproliferative activity in Daudi, WISH,
and primary human lymphocyte cells
exhibiting approximately 6 times higher
anti-proliferative activity than either
parent IFN. These IFN hybrids provide
a powerful tool for studying the
structure-function relationship of these
molecules. The engineered IFN-alpha
proteins may have important new
therapeutic applications and may
provide greater insights into
understanding of the clinical activities
of existing IFN-alphas.
Also available for licensing are hybrid
INF-alpha nucleic acids encoding the
hybrid polypeptides as well as cells,
vectors, pharmaceutical compositions
with these nucleic acid sequences.
Potential Commercial Applications
• Anti-viral and cancer therapeutics
• Research tool to study IFN-alpha
functions
Competitive Advantages
Notice.
SUMMARY:
PO 00000
46309
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• Ease of manufacture
• Strong anti-viral activity
Development Stage: In vitro data
available.
Inventors: Kathryn C. Zoon (NIAID),
Joseph B. Bekisz (NIAID), Mark P. Hayes
(FDA), Renqiu Hu (FDA).
Publications
1. Hu R, et al. Protein engineering of
interferon alphas. Methods Mol Med.
2005;116:69–80. [PMID 16000855]
2. Hu R, et al. Human IFN-alpha protein
engineering: the amino acid residues at
positions 86 and 90 are important for
antiproliferative activity. J Immunol.
2001 Aug 1;167(3):1482–9. [PMID
11466368]
3. Hu R, et al. Divergence of binding,
signaling, and biological responses to
recombinant human hybrid IFN. J
Immunol. 1999 Jul 15;163(2):854–60.
[PMID 10395679]
Intellectual Property: HHS Reference
No. E–068–1998/0—
• US Patent No. 6,685,933 issued 03
Feb 2004
• US Patent No. 7,235,232 issued 26 Jun
2007
Licensing Contact: Peter Soukas; 301–
435–4646; ps193c@nih.gov.
Novel Treatment for Anemia and
Polycythemia: AVPR1B Molecules
Modulating Erythropoiesis
Description of Technology: Anemia
can be caused by chronic diseases,
chemotherapy, or radiation.
Erythropoietin is commonly used to
stimulate red blood cell production for
anemia treatment, but it takes about a
week to manifest its clinical effect. The
E:\FR\FM\04AUN1.SGM
04AUN1
46310
Federal Register / Vol. 80, No. 149 / Tuesday, August 4, 2015 / Notices
subject invention describes the arginine
vasopressin receptor 1B (AVPR1B)
stimulatory molecules that can be used
to stimulate hematopoietic stem cell
proliferation. Preliminary results from
animal studies suggest that the number
of red blood cells and their precursors
significantly increased on day 2
following AVP administration, an onset
time much faster than erythropoietin.
The AVPR1B stimulatory molecules can
be used to jumpstart the system and
erythropoietin can be used to sustain
the effect. In addition, the AVPR1B
inhibitory molecules can be used to
suppress hematopoietic stem cell
proliferation to treat polycythemia
(overproduction of red blood cells).
Potential Commercial Applications
• Treatment of anemia caused by
chronic diseases, chemotherapy, or
radiation.
• Anemia patients who do not
respond to erythropoietin.
• Polycythemia treatment.
Competitive Advantages: AVPR1B
stimulatory molecules act faster than the
commonly used erythropoietin for
anemia treatment.
are among the most frequently used
viral vectors for gene therapy because
AAV vectors can infect both dividing
and non-dividing cells, and can
establish long-term transgene
expression. Two major issues in gene
therapy are the ability to efficiently
transduce the target cells and to evade
the immune response to vectors. The
subject invention describes a mutated
AAV serotype 5 by modifying sialic acid
binding regions which mediate viral
entry into host cells. Preliminary results
from animal studies suggest that this
modification can increase transduction
by 3–4 folds in salivary glands and
muscle, and can significantly decrease
the potential of being neutralized by
preexisting antibodies compared to the
wild type. Thus, the modified AAV5
vectors seem to be optimal for gene
therapy.
Potential Commercial Applications:
Genetically engineered AAV5 vectors
for gene therapy.
Competitive Advantages
• Enhanced transduction activity.
• Reduced the potential for being
neutralized by preexisting antibodies.
Development Stage
• Early-stage
• In vivo data available (animal)
Inventors: Eva Mezey and Miklos
Krepuska (NIDCR); Balazs Mayer and
Krisztian Nemeth (Semmelweis
University Medical School)
Intellectual Property: HHS Reference
No. E–619–2013/0—
• US Application No. 61/885,258 filed
October 01, 2013 (E–619–2013/0–US–
01)
• PCT Application No. PCT/US2014/
058613 filed October 01, 2014 (E–
619–2013/0–PCT–02)
Licensing Contact: Sally Hu, Ph.D.,
M.B.A.; 301–435–5605; hus@
mail.nih.gov.
Collaborative Research Opportunity:
The National Institute of Dental and
Craniofacial Research is seeking
statements of capability or interest from
parties interested in collaborative
research to further develop, evaluate or
commercialize treatment for anemia and
polycythemia. For collaboration
opportunities, please contact David
Bradley, Ph.D. at bradleyda@
nidcr.nih.gov.
tkelley on DSK3SPTVN1PROD with NOTICES
Development Stage
• Early-stage
• In vivo data available (animal)
Inventors: John Chiorini and Sandra
Afione-Wainer (NIDCR); Mavis
Agbandje-Mckenna and Sujata Halder
(University of Florida).
Modified AAV5 Vectors for Enhanced
Transduction and Reduced Antibody
Neutralization
Description of Technology: Adenoassociated viruses (AAVs) are small
nonpathogenic viruses and can integrate
into the cellular genome. AAV vectors
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Publications
1. Afione S, et al. Identification and
mutagenesis of the adeno-associated
virus 5 sialic acid binding region. J Virol.
2015 Feb; 89(3): 1660–72. [PMID
25410855]
2. Chiorini J, et al. AAV4 Vector and the uses
thereof. U.S. Patent 6,468,524, issued on
October 22, 2002.
3. Chiorini J, et al. AAV5 Vector and the uses
thereof. U.S. Patent 7,479,554, issued
January 20, 2009, and U.S. Patent
6.984,517, issued on January 10, 2006.
4. Chiorini J, et al. AAV5 Vector for
transducing brain cells and lung cells.
U.S. Patent 6,855,314, issued on
February 15, 2005.
Intellectual Property: HHS Reference
No. E–097–2015/0—US Application No.
62/143,524 filed April 6, 2015.
Related Technologies
• E–175–2015: US 62/160,552.
• E–736–2013: PCT/US14/59825.
• E–142–2011 family: PCT/US12/
34268, CA, EP and US.
• E–087–2011 family: PCT/US12/
33556, EP and US.
• E–232–2011: US 14/428,929.
• E–194–2010: US 8,808,684.
• E–179–2005: US 8,283,151.
PO 00000
Frm 00077
Fmt 4703
Sfmt 4703
• E–227–2004: US 7,407,801.
• E–329–2003 family: US 8,137,960,
US 8,685,722.
• E–105–2003: US 8,927,269.
• E–308–2001: US 7,419,817.
• E–071–2000: US 6,468,524.
• E–127–1998 family: US 6,984,517,
AU, CA, EP, and JP.
Licensing Contact: Sally Hu, Ph.D.,
M.B.A.; 301–435–5606; hus@
mail.nih.gov.
Collaborative Research Opportunity:
The National Institute of Dental and
Craniofacial Research is seeking
statements of capability or interest from
parties interested in collaborative
research to further develop, evaluate or
commercialize modified AAV5 vector
for gene therapy. For collaboration
opportunities, please contact David
Bradley, Ph.D. at bradleyda@
nidcr.nih.gov.
A Novel Adeno-Associated Virus for
Gene Therapy
Description of Technology: Adenoassociated viruses (AAVs) are small
nonpathogenic viruses and can integrate
into the cellular genome. AAV vectors
are among the most frequently used
viral vectors for gene therapy because
AAV vectors can infect both dividing
and non-dividing cells, and can
establish long-term transgene
expression. The subject invention
describes a novel AAV termed ‘‘44–9.’’
AAV44–9 based vectors have high gene
transfer activity in a number of cell
types, including salivary gland cells,
liver cells, and different types of
neurons (e.g., cells of the cortex,
olfactory bulb, and brain stem, and
Purkinje cells of the cerebellum). These
vectors can deliver heterologous genes
to particular target cells through sitespecific administration. Preliminary
results from animal studies suggest that
AAV44–9 vectors can efficiently deliver
genes of interest, and the protein
products of the delivered genes can be
detected in bloodstream and at the local
tissues. Therefore, these vectors are
suitable for gene therapy for cells/
tissues that are not efficiently targeted
by other vectors.
Potential Commercial Applications:
AAV44–9 can be used as a delivery
vector in gene therapy.
Competitive Advantages
• High gene transfer activity in a
number of cell types including salivary
gland cells, liver cells, and different
types of neurons (e.g., cells of the
cortex, olfactory bulb, and brain stem,
and Purkinje cells of the cerebellum).
• As a gene transfer vector for cells
that are not efficiently targeted by other
vector.
E:\FR\FM\04AUN1.SGM
04AUN1
Federal Register / Vol. 80, No. 149 / Tuesday, August 4, 2015 / Notices
Development Stage
• In vitro data available
• In vivo data available (animal)
Inventors: John Chiorini and Giovanni
Pasquale (NIDCR).
Publication: Schmidt M, et al.
Identification and characterization of
novel adeno-associated virus isolates in
ATCC virus stocks. J Virol. 2006 May;
80 (10): 5082–5098. [PMID 16641301]
Intellectual Property: HHS Reference
No. E–175–2015/0—US Application No.
62/160,552 filed May 12, 2015.
tkelley on DSK3SPTVN1PROD with NOTICES
Related Technologies
• E–097–2015: US 62/143,524.
• E–736–2013: PCT/US14/59825.
• E–142–2011 family: PCT/US12/
34268, CA, EP and US.
• E–087–2011 family: PCT/US12/
33556, EP and US.
• E–232–2011: US 14/428,929.
• E–194–2010: US 8,808,684.
• E–179–2005: US 8,283,151.
• E–227–2004: US 7,407,801.
• E–329–2003 family: US 8,137,960,
US 8,685,722.
• E–105–2003: US 8,927,269.
• E–308–2001: US 7,419,817.
• E–071–2000: US 6,468,524.
• E–127–1998 family: US 6,984,517,
AU, CA, EP, and JP.
Licensing Contact: Sally Hu, Ph.D.,
M.B.A.; 301–435–5606; hus@
mail.nih.gov.
Collaborative Research Opportunity:
The National Institute of Dental and
Craniofacial Research is seeking
statements of capability or interest from
parties interested in collaborative
research to further develop, evaluate or
commercialize AAV44–9 vector for gene
therapy. For collaboration
opportunities, please contact David
Bradley, Ph.D. at bradleyda@
nidcr.nih.gov.
WNT1-Induced Secreted Protein-1
Knockout Mouse Model
Description of Technology: WNT1induced secreted protein-1 (WISP1) is
expressed at high levels in osteoblasts
and their precursors. WIPS1 plays an
important role in various aspects of
bone formation. Scientists at the NIH
generated Wisp1-deficient (Wisp1-/-)
mice. Deletion of Wisp1 resulted in a
decrease in bone mineral density, total
bone volume, bone thickness, and
biomechanical strength. Wisp1
knockout mouse model can be used to
study the molecular mechanisms of
bone turnover and patho/physiology of
tissues that express WISP1.
Potential Commercial Applications
• To study the molecular mechanisms
of bone formation and
osteodifferentiation.
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• To study the patho/physiology of
tissues that express WISP1, including
cartilage during osteoarthritis, healing
skin, and other soft tissues including
lung, pancreas, and heart.
Development Stage: In vivo data
available (animal).
Inventors: Marian F. Young, Mitsuaki
Ono, Azusa Maeda (all of NIDCR).
Publication: Maeda A, et al. WNT1induced secreted protein-1 (WISP1), a
novel regulator of bone turnover and
Wnt signaling. J Bio Chem. 2015 May
29;290(22):14004–18. [PMID 25864198]
Intellectual Property: HHS Reference
No. E–234–2015/0—Research Tool.
Patent protection is not being pursued
for this technology.
Licensing Contact: Sally Hu, Ph.D.,
M.B.A.; 301–435–5606; hus@
mail.nih.gov
Collaborative Research Opportunity:
The National Institute of Dental and
Craniofacial Research is seeking
statements of capability or interest from
parties interested in collaborative
research to further develop, evaluate or
commercialize WNT1-Induced Secreted
Protein-1 Knockout Mouse Model. For
collaboration opportunities, please
contact David Bradley, Ph.D. at
bradleyda@nidcr.nih.gov.
Dated: July 30, 2015.
Richard U. Rodriguez,
Acting Director, Office of Technology
Transfer, National Institutes of Health.
[FR Doc. 2015–19082 Filed 8–3–15; 8:45 am]
BILLING CODE 4140–01–P
DEPARTMENT OF HEALTH AND
HUMAN SERVICES
46311
Emphasis Panel; Review of U24 Applications
for Parkinson’s Disease Repositories.
Date: August 11, 2015.
Time: 9:00 a.m. to 1:00 p.m.
Agenda: To review and evaluate grant
applications.
Place: National Institutes of Health,
Neuroscience Center, 6001 Executive
Boulevard, Rockville, MD 20852, (Telephone
Conference Call).
Contact Person: Joel A. Saydoff, Ph.D.,
Scientific Review Officer, Scientific Review
Branch, Division of Extramural Research,
NINDS/NIH/DHHS/Neuroscience Center,
6001 Executive Boulevard, Suite 3205, MSC
9529, Bethesda, MD 20892–9529, 301–435–
9223, joel.saydoff@nih.gov.
Name of Committee: National Institute of
Neurological Disorders and Stroke Special
Emphasis Panel; Review of U01 Applications
for Parkinson’s Disease Biomarker Program.
Date: August 12, 2015.
Time: 8:00 a.m. to 12:00 p.m.
Agenda: To review and evaluate grant
applications.
Place: National Institutes of Health,
Neuroscience Center, 6001 Executive
Boulevard, Rockville, MD 20852, (Telephone
Conference Call).
Contact Person: Joel A. Saydoff, Ph.D.,
Scientific Review Officer, Scientific Review
Branch, Division of Extramural Research,
NINDS/NIH/DHHS/Neuroscience Center,
6001 Executive Boulevard, Suite 3205, MSC
9529, Bethesda, MD 20892–9529, 301–435–
9223.
(Catalogue of Federal Domestic Assistance
Program Nos. 93.853, Clinical Research
Related to Neurological Disorders; 93.854,
Biological Basis Research in the
Neurosciences, National Institutes of Health,
HHS)
Dated: July 29, 2015.
Carolyn Baum,
Program Analyst, Office of Federal Advisory
Committee Policy.
[FR Doc. 2015–19032 Filed 8–3–15; 8:45 am]
National Institutes of Health
BILLING CODE 4140–01–P
National Institute of Neurological
Disorders and Stroke: Notice of Closed
Meetings
DEPARTMENT OF HEALTH AND
HUMAN SERVICES
Pursuant to section 10(d) of the
Federal Advisory Committee Act, as
amended (5 U.S.C. App.), notice is
hereby given of the following meetings.
The meetings will be closed to the
public in accordance with the
provisions set forth in sections
552b(c)(4) and 552b(c)(6), Title 5 U.S.C.,
as amended. The grant applications and
the discussions could disclose
confidential trade secrets or commercial
property such as patentable material,
and personal information concerning
individuals associated with the grant
applications, the disclosure of which
would constitute a clearly unwarranted
invasion of personal privacy.
Name of Committee: National Institute of
Neurological Disorders and Stroke Special
PO 00000
Frm 00078
Fmt 4703
Sfmt 4703
National Institutes of Health
Center for Scientific Review: Notice of
Closed Meeting
Pursuant to section 10(d) of the
Federal Advisory Committee Act, as
amended (5 U.S.C. App.), notice is
hereby given of the following meeting.
The meeting will be closed to the
public in accordance with the
provisions set forth in sections
552b(c)(4) and 552b(c)(6), Title 5 U.S.C.,
as amended. The grant applications and
the discussions could disclose
confidential trade secrets or commercial
property such as patentable material,
and personal information concerning
individuals associated with the grant
applications, the disclosure of which
E:\FR\FM\04AUN1.SGM
04AUN1
Agencies
[Federal Register Volume 80, Number 149 (Tuesday, August 4, 2015)]
[Notices]
[Pages 46309-46311]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 2015-19082]
-----------------------------------------------------------------------
DEPARTMENT OF HEALTH AND HUMAN SERVICES
National Institutes of Health
Government-Owned Inventions; Availability for Licensing
AGENCY: National Institutes of Health, HHS.
ACTION: Notice.
-----------------------------------------------------------------------
SUMMARY: The inventions listed below are owned by an agency of the U.S.
Government and are available for licensing in the U.S. in accordance
with 35 U.S.C. 209 and 37 CFR part 404 to achieve expeditious
commercialization of results of federally-funded research and
development. Foreign patent applications are filed on selected
inventions to extend market coverage for companies and may also be
available for licensing.
FOR FURTHER INFORMATION CONTACT: Licensing information and copies of
the U.S. patent applications listed below may be obtained by writing to
the indicated licensing contact at the Office of Technology Transfer,
National Institutes of Health, 6011 Executive Boulevard, Suite 325,
Rockville, Maryland 20852-3804; telephone: 301-496-7057; fax: 301-402-
0220. A signed Confidential Disclosure Agreement will be required to
receive copies of the patent applications.
SUPPLEMENTARY INFORMATION: Technology descriptions follow.
Interferon Alpha Hybrids
Description of Technology: Available for licensing are hybrid
interferon alpha (INF-alpha) polypeptides constructed by combinations
of INFalpha21b and INFalpha2c, and mutants of these hybrids. These
hybrid constructs have resulted in novel IFNs that either combine
different biological properties from the parent proteins or have
significantly different biological activity from both the parents in
anti-proliferative, anti-viral, or competitive binding properties. For
instance, the hybrid designated HY-3 has higher anti-proliferative
activity in Daudi, WISH, and primary human lymphocyte cells exhibiting
approximately 6 times higher anti-proliferative activity than either
parent IFN. These IFN hybrids provide a powerful tool for studying the
structure-function relationship of these molecules. The engineered IFN-
alpha proteins may have important new therapeutic applications and may
provide greater insights into understanding of the clinical activities
of existing IFN-alphas.
Also available for licensing are hybrid INF-alpha nucleic acids
encoding the hybrid polypeptides as well as cells, vectors,
pharmaceutical compositions with these nucleic acid sequences.
Potential Commercial Applications
Anti-viral and cancer therapeutics
Research tool to study IFN-alpha functions
Competitive Advantages
Ease of manufacture
Strong anti-viral activity
Development Stage: In vitro data available.
Inventors: Kathryn C. Zoon (NIAID), Joseph B. Bekisz (NIAID), Mark
P. Hayes (FDA), Renqiu Hu (FDA).
Publications
1. Hu R, et al. Protein engineering of interferon alphas. Methods
Mol Med. 2005;116:69-80. [PMID 16000855]
2. Hu R, et al. Human IFN-alpha protein engineering: the amino acid
residues at positions 86 and 90 are important for antiproliferative
activity. J Immunol. 2001 Aug 1;167(3):1482-9. [PMID 11466368]
3. Hu R, et al. Divergence of binding, signaling, and biological
responses to recombinant human hybrid IFN. J Immunol. 1999 Jul
15;163(2):854-60. [PMID 10395679]
Intellectual Property: HHS Reference No. E-068-1998/0--
US Patent No. 6,685,933 issued 03 Feb 2004
US Patent No. 7,235,232 issued 26 Jun 2007
Licensing Contact: Peter Soukas; 301-435-4646; ps193c@nih.gov.
Novel Treatment for Anemia and Polycythemia: AVPR1B Molecules
Modulating Erythropoiesis
Description of Technology: Anemia can be caused by chronic
diseases, chemotherapy, or radiation. Erythropoietin is commonly used
to stimulate red blood cell production for anemia treatment, but it
takes about a week to manifest its clinical effect. The
[[Page 46310]]
subject invention describes the arginine vasopressin receptor 1B
(AVPR1B) stimulatory molecules that can be used to stimulate
hematopoietic stem cell proliferation. Preliminary results from animal
studies suggest that the number of red blood cells and their precursors
significantly increased on day 2 following AVP administration, an onset
time much faster than erythropoietin. The AVPR1B stimulatory molecules
can be used to jumpstart the system and erythropoietin can be used to
sustain the effect. In addition, the AVPR1B inhibitory molecules can be
used to suppress hematopoietic stem cell proliferation to treat
polycythemia (overproduction of red blood cells).
Potential Commercial Applications
Treatment of anemia caused by chronic diseases,
chemotherapy, or radiation.
Anemia patients who do not respond to erythropoietin.
Polycythemia treatment.
Competitive Advantages: AVPR1B stimulatory molecules act faster
than the commonly used erythropoietin for anemia treatment.
Development Stage
Early-stage
In vivo data available (animal)
Inventors: Eva Mezey and Miklos Krepuska (NIDCR); Balazs Mayer and
Krisztian Nemeth (Semmelweis University Medical School)
Intellectual Property: HHS Reference No. E-619-2013/0--
US Application No. 61/885,258 filed October 01, 2013 (E-619-
2013/0-US-01)
PCT Application No. PCT/US2014/058613 filed October 01, 2014
(E-619-2013/0-PCT-02)
Licensing Contact: Sally Hu, Ph.D., M.B.A.; 301-435-5605;
hus@mail.nih.gov.
Collaborative Research Opportunity: The National Institute of
Dental and Craniofacial Research is seeking statements of capability or
interest from parties interested in collaborative research to further
develop, evaluate or commercialize treatment for anemia and
polycythemia. For collaboration opportunities, please contact David
Bradley, Ph.D. at bradleyda@nidcr.nih.gov.
Modified AAV5 Vectors for Enhanced Transduction and Reduced Antibody
Neutralization
Description of Technology: Adeno-associated viruses (AAVs) are
small nonpathogenic viruses and can integrate into the cellular genome.
AAV vectors are among the most frequently used viral vectors for gene
therapy because AAV vectors can infect both dividing and non-dividing
cells, and can establish long-term transgene expression. Two major
issues in gene therapy are the ability to efficiently transduce the
target cells and to evade the immune response to vectors. The subject
invention describes a mutated AAV serotype 5 by modifying sialic acid
binding regions which mediate viral entry into host cells. Preliminary
results from animal studies suggest that this modification can increase
transduction by 3-4 folds in salivary glands and muscle, and can
significantly decrease the potential of being neutralized by
preexisting antibodies compared to the wild type. Thus, the modified
AAV5 vectors seem to be optimal for gene therapy.
Potential Commercial Applications: Genetically engineered AAV5
vectors for gene therapy.
Competitive Advantages
Enhanced transduction activity.
Reduced the potential for being neutralized by preexisting
antibodies.
Development Stage
Early-stage
In vivo data available (animal)
Inventors: John Chiorini and Sandra Afione-Wainer (NIDCR); Mavis
Agbandje-Mckenna and Sujata Halder (University of Florida).
Publications
1. Afione S, et al. Identification and mutagenesis of the adeno-
associated virus 5 sialic acid binding region. J Virol. 2015 Feb;
89(3): 1660-72. [PMID 25410855]
2. Chiorini J, et al. AAV4 Vector and the uses thereof. U.S. Patent
6,468,524, issued on October 22, 2002.
3. Chiorini J, et al. AAV5 Vector and the uses thereof. U.S. Patent
7,479,554, issued January 20, 2009, and U.S. Patent 6.984,517,
issued on January 10, 2006.
4. Chiorini J, et al. AAV5 Vector for transducing brain cells and
lung cells. U.S. Patent 6,855,314, issued on February 15, 2005.
Intellectual Property: HHS Reference No. E-097-2015/0--US
Application No. 62/143,524 filed April 6, 2015.
Related Technologies
E-175-2015: US 62/160,552.
E-736-2013: PCT/US14/59825.
E-142-2011 family: PCT/US12/34268, CA, EP and US.
E-087-2011 family: PCT/US12/33556, EP and US.
E-232-2011: US 14/428,929.
E-194-2010: US 8,808,684.
E-179-2005: US 8,283,151.
E-227-2004: US 7,407,801.
E-329-2003 family: US 8,137,960, US 8,685,722.
E-105-2003: US 8,927,269.
E-308-2001: US 7,419,817.
E-071-2000: US 6,468,524.
E-127-1998 family: US 6,984,517, AU, CA, EP, and JP.
Licensing Contact: Sally Hu, Ph.D., M.B.A.; 301-435-5606;
hus@mail.nih.gov.
Collaborative Research Opportunity: The National Institute of
Dental and Craniofacial Research is seeking statements of capability or
interest from parties interested in collaborative research to further
develop, evaluate or commercialize modified AAV5 vector for gene
therapy. For collaboration opportunities, please contact David Bradley,
Ph.D. at bradleyda@nidcr.nih.gov.
A Novel Adeno-Associated Virus for Gene Therapy
Description of Technology: Adeno-associated viruses (AAVs) are
small nonpathogenic viruses and can integrate into the cellular genome.
AAV vectors are among the most frequently used viral vectors for gene
therapy because AAV vectors can infect both dividing and non-dividing
cells, and can establish long-term transgene expression. The subject
invention describes a novel AAV termed ``44-9.'' AAV44-9 based vectors
have high gene transfer activity in a number of cell types, including
salivary gland cells, liver cells, and different types of neurons
(e.g., cells of the cortex, olfactory bulb, and brain stem, and
Purkinje cells of the cerebellum). These vectors can deliver
heterologous genes to particular target cells through site-specific
administration. Preliminary results from animal studies suggest that
AAV44-9 vectors can efficiently deliver genes of interest, and the
protein products of the delivered genes can be detected in bloodstream
and at the local tissues. Therefore, these vectors are suitable for
gene therapy for cells/tissues that are not efficiently targeted by
other vectors.
Potential Commercial Applications: AAV44-9 can be used as a
delivery vector in gene therapy.
Competitive Advantages
High gene transfer activity in a number of cell types
including salivary gland cells, liver cells, and different types of
neurons (e.g., cells of the cortex, olfactory bulb, and brain stem, and
Purkinje cells of the cerebellum).
As a gene transfer vector for cells that are not
efficiently targeted by other vector.
[[Page 46311]]
Development Stage
In vitro data available
In vivo data available (animal)
Inventors: John Chiorini and Giovanni Pasquale (NIDCR).
Publication: Schmidt M, et al. Identification and characterization
of novel adeno-associated virus isolates in ATCC virus stocks. J Virol.
2006 May; 80 (10): 5082-5098. [PMID 16641301]
Intellectual Property: HHS Reference No. E-175-2015/0--US
Application No. 62/160,552 filed May 12, 2015.
Related Technologies
E-097-2015: US 62/143,524.
E-736-2013: PCT/US14/59825.
E-142-2011 family: PCT/US12/34268, CA, EP and US.
E-087-2011 family: PCT/US12/33556, EP and US.
E-232-2011: US 14/428,929.
E-194-2010: US 8,808,684.
E-179-2005: US 8,283,151.
E-227-2004: US 7,407,801.
E-329-2003 family: US 8,137,960, US 8,685,722.
E-105-2003: US 8,927,269.
E-308-2001: US 7,419,817.
E-071-2000: US 6,468,524.
E-127-1998 family: US 6,984,517, AU, CA, EP, and JP.
Licensing Contact: Sally Hu, Ph.D., M.B.A.; 301-435-5606;
hus@mail.nih.gov.
Collaborative Research Opportunity: The National Institute of
Dental and Craniofacial Research is seeking statements of capability or
interest from parties interested in collaborative research to further
develop, evaluate or commercialize AAV44-9 vector for gene therapy. For
collaboration opportunities, please contact David Bradley, Ph.D. at
bradleyda@nidcr.nih.gov.
WNT1-Induced Secreted Protein-1 Knockout Mouse Model
Description of Technology: WNT1-induced secreted protein-1 (WISP1)
is expressed at high levels in osteoblasts and their precursors. WIPS1
plays an important role in various aspects of bone formation.
Scientists at the NIH generated Wisp1-deficient (Wisp1-/-) mice.
Deletion of Wisp1 resulted in a decrease in bone mineral density, total
bone volume, bone thickness, and biomechanical strength. Wisp1 knockout
mouse model can be used to study the molecular mechanisms of bone
turnover and patho/physiology of tissues that express WISP1.
Potential Commercial Applications
To study the molecular mechanisms of bone formation and
osteodifferentiation.
To study the patho/physiology of tissues that express
WISP1, including cartilage during osteoarthritis, healing skin, and
other soft tissues including lung, pancreas, and heart.
Development Stage: In vivo data available (animal).
Inventors: Marian F. Young, Mitsuaki Ono, Azusa Maeda (all of
NIDCR).
Publication: Maeda A, et al. WNT1-induced secreted protein-1
(WISP1), a novel regulator of bone turnover and Wnt signaling. J Bio
Chem. 2015 May 29;290(22):14004-18. [PMID 25864198]
Intellectual Property: HHS Reference No. E-234-2015/0--Research
Tool. Patent protection is not being pursued for this technology.
Licensing Contact: Sally Hu, Ph.D., M.B.A.; 301-435-5606;
hus@mail.nih.gov
Collaborative Research Opportunity: The National Institute of
Dental and Craniofacial Research is seeking statements of capability or
interest from parties interested in collaborative research to further
develop, evaluate or commercialize WNT1-Induced Secreted Protein-1
Knockout Mouse Model. For collaboration opportunities, please contact
David Bradley, Ph.D. at bradleyda@nidcr.nih.gov.
Dated: July 30, 2015.
Richard U. Rodriguez,
Acting Director, Office of Technology Transfer, National Institutes of
Health.
[FR Doc. 2015-19082 Filed 8-3-15; 8:45 am]
BILLING CODE 4140-01-P